Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phenomenon of natriuresis during the early phase of total starvation has been described in man and rabbit. We have examined the pattern of electrolyte excretion initiated by starvation for 4 days in the male Wistar rat. Within 24 hr sodium excretion is significantly diminished when compared to prestarvation values (control 2.55 +/- 0.76 [S.D.] mEq/day; 1-day fast 0.42 +/- 0.27) and by day 2 is less than one tenth of the control value. Chloride retention parallels this sodium conservation. Concomitant changes in urinary pH and ammonia excretion (UNH4V) reflect the mild acidosis of starvation (control pH 7.46 +/- 0.18 [S.D.], UNH4V 0.21 +/- 0.08 [S.D.] mEq/day; day 2 pH 6.10 +/- 0.31, UNH4V 0.71 +/- 0.21). However, the excretion of organic acids is not elevated but is actually decreased by day 2 (control 1.02 +/- 0.21 [S.D.] mEq/day; day 2 0.66 +/- 0.26). The majority of the organic acids are excreted as salts (day-2 0.51 +/- 0.21). This level of excretion does not obligate excessive sodium loss and can be adequately matched by renal ammonia production. Normal plasma glucose levels are maintained, consistent with the well-documented increase in renal gluconeogenesis in the starved rat. Plasma levels of glucagon, a known natriuretic and ketogenic agent, do not rise, and this together with a normal plasma glucose concentration may account for the failure of the rat to exhibit the natriuresis of starvation that is observed in man and rabbit.
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PMID:Renal sodium conservation during starvation in the rat. 64 88

An investigation was carried out in conscious dogs concerning the effects of three adenosine derivatives substituted at the 5'-(744-96) or 2'-, 3'-, and 5'-positions (744-98, 744-99), with pronounced and long-lasting coronary dilator activity, on glucagon release. All three compounds (10 microgram/kg i.v.) induced a sustained increase in plasma glucose and a decrease in plasma FFA concentration; concomitantly, plasma glucagon levels rose 2--3 fold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. A lowering of blood pressure of similar magnitude by sodium nitroprusside infusion in control experiments failed to show any significant effect on plasma glucagon level. These results point to a specific effect of vasoactive adenosine derivatives on glucagon release.
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PMID:Evidence for glucagon-releasing activity of vasoactive adenosine analogues in the conscious dog. 71 81

Intravenous glucagon and diuresis caused by diagnostic doses of sodium diatrizoate were used to treat 5 patients with ureteral colic and urographic findings consistent with partial obstruction by a ureteral calculus. Pain was relieved and the calculus passed within two hours in 4 patients and within eight hours in the fifth. No complications were noted.
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PMID:Glucagon and diuresis in the treatment of ureteral calculi. 72 63

The effects of glucagon, gastric inhibitory peptide (GIP), and secretin on the concentrating mechanism and the motility in the feline gallbladder have been studied in vivo. A technique by which the gallbladder in situ was perfused by an electrolyte solution made possible a simultaneous study of the motility and of the net transport of water and electrolytes across the gallbladder wall. Secretin (0.6 microgram per kg/h) was found to abolish the net absorption of water, Na+, and HCO3- and strongly reduce the net absorption of K+ and Cl-, whereas neither glucagon (1--20 microgram per kg/h) nor GIP (1--30 microgram per kg/h) was found to significantly influence the concentrating function of the gallbladder. The motility of the gallbladder was not influenced by the peptides. The formation of bile and pancreatic secretion was not changed by glucagon or GIP, whereas secretin had a potent effect.
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PMID:A comparison of glucagon, gastric inhibitory peptide, and secretin on gallbladder function, formation of bile, and pancreatic secretion in the cat. 72 15

1. Arrhenius plots of the glucagon-stimulated adenylate cyclase, 5'-nucleotidase, (Na+ + K+)-stimulated adenosine triphosphatase and Mg2+-dependent adenosine triphosphatase activities of control hamster liver plasma membranes exhibited two break points at around 25 and 13 degrees C, whereas Arrhenius plots of their activities in hibernating hamster liver plasma membranes exhibited two break points at around 25 and 4 degrees C. 2. A single break occurring between 25 and 26 degrees C was observed in Arrhenius plots of the activities of fluoride-stimulated adenylate cyclase, basal adenylate cyclase and cyclic AMP phosphodiesterase of liver plasma membranes from both control and hibernating animals. 3. Arrhenius plots of phosphodiesterase I activity showed a single break at 13 degrees C for membranes from control animals, and a single break at around 4 degrees C for liver plasma membranes from hibernating animals. 4. The temperature at which break points occurred in Arrhenius plots of glucagon- and fluoride-stimulated adenylate cyclase activity were decreased by about 7--8 degrees C by addition of 40 mm-benzyl alcohol to the assays. 5. Discontinuities in the Arrhenius plots of 4-anilinonaphthalene-1-sulphonic acid fluorescence occurred at around 24 and 13 degrees C for liver plasma membranes from control animals, and at around 25 and 4 degrees C for membranes from hibernating animals. 6. We suggest that in hamster liver plasma membranes from control animals a lipid phase separation occurs at around 25 degrees C in the inner half of the bilayer and at around 13 degrees C in the outer half of the bilayer. On hibernation a change in bilayer asymmetry occurs, which is expressed by a decrease in the temperature at which the lipid phase separation occurs in the outer half of the bilayer to around 4 degrees C. The assumption made is that enzymes expressing both lipid phase separations penetrate both halves of the bilayer, whereas those experiencing a single break penetrate one half of the bilayer only.
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PMID:Changes in the form of Arrhenius plots of the activity of glucagon-stimulated adenylate cyclase and other hamster liver plasma-membrane enzymes occurring on hibernation. 72 95

1. Isolated segments of mouse liver were placed in a Perspex bath through which physiological saline solutions of varying composition were circulated. Two microelectrodes were inserted in different liver cells under microscopic control allowing measurement of distance between the two micro-electrode tips. Current pulses were injected through one of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the second micro-electrode. The spatial decrement of the amplitude of the electrotonzpotential changes and their dependence on extracellular ion concentrations were analysed by three-dimensional cable analysis, modified to account for the geometry of the tissue. 2. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (lambda3 = square root of Rm/chrRi) was 390 micron and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 komegacm. From these values, and an estimate of tissue cell membrane density (chi) obtained by others, the specific membrane resistance (Rm) was calculated to be 5.1 komegacm2. 3. Replacement of extracellular Na+ by K+ resulted in a large depolarization and a large decrease in the membrane resistance. Replacement of extracellular Na+ by choline resulted in a small transient hyperpolarization and a small increase in the membrane resistance. Replacement of extracellular Cl- by methylsulphate or sulphate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. 4. Glucagon (10(-7) M) and adrenaline (10(-5) M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). 5. The resting membrane ion conductance can be considered to consist of three components, Cl conductance (GCl), GK and GNa. The results suggest that GCl greater than GK greater than GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be explained in part by an increase in GK.
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PMID:Cell membrane potential and resistance in liver. 73 53

In the anaesthetized fasted non-diabetic male intact rat, alrestatin sodium injected as a bolus (0.75 mmol/kg, i.v.) did not affect basal plasma insulin or glucose levels. However, in response to an intravenous glucose tolerance test, plasma insulin levels were significantly increased above the values observed in the animal during a control test. The decreases in plasma glucose levels after alrestatin were significantly greater than in the control study. In rat pancreatic preparations in vitro, alrestatin lowered the basal release of 3H-norepinephrine and also the release obtained with the catecholamine-releasing agent tyramine. A modulation of catecholamine release appears to be of importance in the mode of action of alrestatin with respect to the insulin secretion and plasma glucose levels. It is suggested that alrestatin may play a useful role in the therapy of diabetes mellitus since it can augment insulin secretion when glucose is administered to a fasted animal in which the acute insulin response has been shown to be like that of the human diabetic, and in addition, can lower arginine-stimulated glucagon secretion in the animal, the latter being a model of an action that is observed in the human diabetic. The net effect of these hormonal changes has been predicted previously to be a lowering of the blood glucose levels in the human diabetic patient.
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PMID:Effect of alrestatin sodium on glucose-stimulated insulin secretion in the fasted anaesthetized rat. 74 68

Eighteen diabetic patients with lactic acidosis (L.A.) were analyzed for possible causal factors, metabolic changes, and efficacy of treatment. An antecedent phenformin therapy was performed in fifteen cases and was associated with renal insufficiency in ten cases and liver disease in eight cases. Tissular anoxia of primary hemodynamic or respiratory origin was absent in all cases. The severe metabolic acidosis (pH m.93 +/- 0,03; HCO3-= 6 +/- 1 MM; PaCO2 = 18 +/- 2 MM. Hg) and hyperlactatemia (14.2 +/- 0.3 mM) were associated with high lactate/pyruvate ration (70 +/- 22). High alanine levels (up to 4.6 mM) were measured in some of these patients. High beta-hydroxybutrate levels were sometimes measured (up to 7.6 mM), and substantial amounts of acetoacetate were also detected in twelve cases. Glucagon level was always increased (1,050 +/- 240 pg./ml.), and insulin/glucagon ratio was low. Cortisol (49 +/- 10 mug./100 ml.) and HGH (10.8 +/- 0.6 ng./ml.) were also elevated. Increased plasma levels of phenformin were measured in five L.A. diabetic subjects (50 +/- 5 mug./ml.) by comparison with other phenformin-treated diabetic subjects. The specificity of the assay was investigated, and phenformin metabolites were characterized by thin-layer chromatography. Por the treatment of L.A., adjunction of dialysis and furosemide improved the efficacy of early and massive sodium bicarbonate infusion. It is suggested that accumulation of phenformin via renal insufficiency plays a determinant role in causing L.A. through an impairment of lactate metabolism in the liver. An accelerated epuration of the drug may be helpful in therapy of L.A. Phenformin treatment should be avoided in case of renal and/or liver insufficiency.
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PMID:Phenformin-induced lactic acidosis in diabetic patients. 80 37

To evaluate the effect of physiologic hyperglucagonemia on nitrogen and glucose metabolism and on urinary electrolyte excretion, pancreatic glucagon was administered as a continuous 3-day infusion to three adult-onset non-insulin-dependent diabetics and two insulin-treated juvenile diabetics while on a constant dietary intake. The glucagon infusion resulted in increases in plasma glucagon which were 4-6 fold greater than control values. Despite prolonged hyperglucagonemia, urinary glucose excretion was unchanged. Similarly, urinary urea nitrogen and total nitrogen excretion were not altered by glucagon administration. Urinary sodium tended to rise, albeit not significantly (p less than .01), on the first infusion day, but later declined to control values despite increasing plasma glucagon concentrations. Urinary chloride, potassium, calcium, phosphorus excretion remained unchanged. We conclude that continuous physiologic increments in plasma glucagon do not enhance glycosuria or increase protein catabolism and ureagenesis in diabetes when insulin is available. The augmented protein catabolism and glucogenesis that accompany diabetic ketoacidosis cannot be explained primarily on the basis of hyperglucagonemia.
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PMID:Influence of physiologic hyperglucagonemia on urinary glucose, nitrogen, and electrolyte excretion in diabetes. 83 43

The circulatory response of the kidney to drugs is conditioned by a variety of factors, such as basal vascular tone, dietary sodium and structural changes in the renal vasculature which accompany aging and disease. In addition, any drug which affects systemic arterial pressure will activate renal autoregulatory processes, which are superimposed upon the direct effects of the drug on the renal circulation. Renal autoregulation in addition to passive pressure effects probably accounts for the relative constancy of renal blood flow during the administration of renal vasodilators such as nitroprusside, diazoxide and minoxidil. Renal vasodilators which have minor effects on systemic arterial pressure, such as dopamine and glucagon, increase renal blood flow. These effects have been employed clinically in low cardiac output states. A variety of drugs affect the renal circulation by modifying the effects of endogenous vasoactive substances. The mechanisms of action include: receptor blockade; ex, adrenergic and Ag II-mediated vasoconstriction: enhanced production by the administration of biochemical precursors; ex, arachidonic acid and I-dopa: inhibition of endogenous production; ex, prostaglandin synthetase inhibitors: and inhibition of breakdown of endogenous substances; ex, converting enzyme inhibition. The effect of each of these interventions will depend in part upon the rate of endogenous production of the relevant vasoactive material. The administration of diuretics affects renal blood flow in individually distinctive ways, the mechanisms of which have been only partially elucidated.
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PMID:Pharmacology of the renal circulation. 85 Nov 21


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